Dental Caries, Race and Incident Ischemic Stroke, Coronary Heart Disease, and Death.

BACKGROUND: Dental caries is a highly prevalent disease worldwide. In the United States, untreated dental caries is present in >1 in 5 adults. The objective of this study was to determine the relationship between dental caries and incident ischemic stroke, coronary heart disease (CHD) events, and death. METHODS: The dental cohort (n=6351) of the ARIC study (Atherosclerosis Risk in Communities) was followed for incident ischemic stroke, CHD event, and all-cause mortality. Of all the participants at visit 4 (n=11 656), those who were unable to go through dental examination, or with prevalent ischemic stroke and CHD events, were excluded. The full-mouth dental examination was conducted at visit 4 (1996-1998), assessing dental caries. The dose response of decayed, missing, and filled surfaces due to caries was assessed and related to the outcome. Outcomes were assessed through the end of 2019. Additionally, the effect of regular dental care utilization on dental caries was evaluated. RESULTS: Participants with ≥1 dental caries had an increased risk of stroke (adjusted hazard ratio [HR], 1.40 [95% CI, 1.10-1.79]) and death (adjusted HR, 1.13 [95% CI, 1.01-1.26]) but not for CHD events (adjusted HR, 1.13 [95% CI, 0.93-1.37]). The association of dental caries and ischemic incident stroke was significantly higher in the African American population compared with the White subgroup (interaction term P=0.0001). Increasing decayed, missing, and filled surfaces were significantly associated with stroke (adjusted HR, 1.006 [95% CI, 1.001-1.011]) and death (adjusted HR, 1.003 [95% CI, 1.001-1.005]) but not CHD (adjusted HR, 1.002 [95% CI, 1.000-1.005]). Regular dental care utilization lowered (adjusted odds ratio, 0.19 [95% CI, 0.16-0.22]; P<0.001) the chance of caries. CONCLUSIONS: Among the cohort, dental caries was independently associated with the risk of ischemic stroke and death, with the effect higher in African American participants. Regular dental care utilization was associated with a lower chance of caries, emphasizing its relevance in the prevention of these events.

Periodontal Disease Treatment After Stroke or Transient Ischemic Attack: The PREMIERS Study, a Randomized Clinical Trial.

BACKGROUND: Patients with stroke/transient ischemic attack and periodontal disease (PD) are at increased risk for cardiovascular events. PD treatments that can improve stroke risk factors were tested if they might assist patients with cerebrovascular disease. METHODS: In this multicenter phase II trial, patients with stroke/transient ischemic attack and moderately severe PD were randomly assigned to intensive or standard PD treatment arms. The primary outcome measure was a composite of death, myocardial infarction, and recurrent stroke, as well as adverse events. Secondary outcome included changes in stroke risk factors. RESULTS: A total of 1209 patients with stroke/transient ischemic attack were screened, of whom 481 met the PD eligibility criteria; 280 patients were randomized to intensive arm (n=140) and standard arm (n=140). In 12-month period, primary outcome occurred in 11 (8%) in the intensive arm and 17 (12%) in the standard arm. The intensive arm was nonsuperior to the standard arm (hazard ratio, 0.65 [95% CI, 0.30-1.38]) with similar rates of adverse events (sepsis 2.1% versus 0.7%; dental bleeding 1.4% versus 0%; and infective endocarditis 0.7% versus 0%). Secondary-outcome improvements were noted in both arms with diastolic blood pressure and high-density lipoprotein cholesterol (P<0.05). CONCLUSIONS: In patients with recent stroke/transient ischemic attack and PD, intensive PD treatment was not superior to standard PD treatment in prevention of stroke/myocardial infarction/death. Fewer events were noted in the intensive arm and the 2 arms were comparable in the safety outcomes. Secondary-outcome measures showed a trend toward improvement, with significant changes noted in diastolic blood pressure and high-density lipoprotein in both the treatment arms.

Periodontal Disease Association with Large-Artery Atherosclerotic Stroke.

OBJECTIVES: We investigated whether periodontal disease is associated with specific stroke subtype. MATERIALS AND METHODS: This is a single-center cross-sectional study. Periodontal disease was assessed in stroke and transient ischemic attack patients. Strokes caused by large-artery atherosclerosis were classified as intracranial atherosclerosis or extracranial atherosclerosis as well as anterior or posterior circulation disease. RESULTS: Consecutive patients (N=265) were enrolled (age 64 ± 12.8, 49% white, 46% black, and 56% male). A third (N=87) had moderately severe periodontal disease. Twenty percent (N=42) were strokes due to large-artery atherosclerosis. Large-artery strokes had a higher proportion of patients with periodontal disease than without periodontal disease (31% vs.16%, X2 p=0.01). There was also a higher proportion of patients with periodontal disease (12% vs. 5%) with stroke due to posterior circulation disease (crude odds ratio or OR 3.0, 95% CI 1.1-7.9, p=0.03), which persisted after adjustment for covariates (adjusted OR 3.1, 95% CI 1.04-9.1, p=0.004). Periodontal disease patients had a higher rate of large-artery stroke due to intracranial atherosclerosis compared to those without periodontal disease (20% vs. 8%; crude OR 2.6, 95% CI 1.3-5.6, p=0.01), and this association persisted after adjustment (adjusted OR 2.6, 95% CI 1.1-5.8, p=0.004). CONCLUSIONS: We report a higher proportion of stroke due to large-artery atherosclerosis in patients with periodontal disease compared to those without periodontal disease. We report an independent association between periodontal disease and intracranial atherosclerosis, as well as between periodontal disease and posterior circulation disease.

Electronic cigarette explosions involving the oral cavity.

BACKGROUND AND OVERVIEW: The use of electronic cigarettes (e-cigarettes) is a rapidly growing trend throughout the United States. E-cigarettes have been linked to the risk of causing explosion and fire. CASE DESCRIPTION: Data are limited on the associated health hazards of e-cigarette use, particularly long-term effects, and available information often presents conflicting conclusions. In addition, an e-cigarette explosion and fire can pose a unique treatment challenge to the dental care provider because the oral cavity may be affected heavily. In this particular case, the patient's injuries included intraoral burns, luxation injuries, and alveolar fractures. CONCLUSIONS AND PRACTICAL IMPLICATIONS: This case report aims to help clinicians gain an increased knowledge about e-cigarette design, use, and risks; discuss the risk of spontaneous failure and explosion of e-cigarettes with patients; and understand the treatment challenges posed by an e-cigarette explosion.

GeneChip microarrays facilitate identification of Protease Nexin-1 as a target gene of the Prx2 (S8) homeoprotein.

The paired-related homeobox genes, Prx1 and Prx2, are important for normal skeletal and cardiovascular development as well as adult vascular remodeling. The identification and characterization of Prx downstream targets is crucial to understanding their function in normal developmental processes and congenital malformations. To identify Prx2 regulated genes, stably transfected NIH3T3 clones expressing Prx2 sense or antisense transcripts were generated. Expression profiles initially were established for two of the clones using Affymetrix GeneChip arrays. Over 6,400 genes were screened by the microarray approach, and approximately 500 genes differed in expression by a factor of two or more. Fifteen genes were chosen for further analysis. RT-PCR of the two transfectants used in the GeneChip analysis demonstrated that five out of the 15 genes were differentially expressed. However, after screening additional stable transfectant clones only one of the 15 genes, Protease Nexin-1 (PN-1), was differentially expressed. Subsequent Northern blot, RT-PCR, and further GeneChip analysis of additional stable transfectants confirmed that PN-1 expression is increased at least fivefold when Prx2 is overexpressed. It was demonstrated that Prx2 directly regulates PN-1 because (1) Prx2 binds to a cis element in the PN-1 promoter in vitro, and (2) Prx2 regulates the PN-1 promoter in transient transfection assays. The GeneChip analysis generated a prioritized list of other potential targets. The utility and limitations of cell culture models combined with microarray analysis for elucidating complex regulatory cascades are discussed.